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{{CMG}}; {{AE}} {{SSW}}
{{CMG}}; {{AE}} {{SSW}}


==Overview==
== Differential Diagnosis ==
__NOTOC__
{| class="wikitable"
! rowspan="2" |S.No.
! rowspan="2" |Disease
! colspan="3" |Symptoms
! colspan="2" |Signs
! colspan="3" |Diagnosis
! rowspan="2" |Comments
|-
!Abdominal Pain
!Hematuria
!Headache
!Abdominal mass
!Abdominal tenderness
!Ultrasonography
!CT scan
!Histology
|-
|1.
|[[Wilms' tumor|Wilms tumor]]
|<nowiki>+</nowiki>
|<nowiki>+ </nowiki>
|<nowiki>-</nowiki>
|<nowiki>+</nowiki>
|<nowiki>+</nowiki>
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*It is the best initial diagnostic study used in cases suspected with wilms tumor.
*Ultrasonography can help identify the mass as a kidney mass.
*It can distinguish tumor mass from other causes of renal swelling like [[hydronephrosis]].<ref name="pmid61529362">{{cite journal |vauthors=Hartman DS, Sanders RC |title=Wilms' tumor versus neuroblastoma: usefulness of ultrasound in differentiation |journal=J Ultrasound Med |volume=1 |issue=3 |pages=117–22 |date=April 1982 |pmid=6152936 |doi= |url=}}</ref>
*Doppler ultrasonography can help to detect invasion of [[renal vein]] and [[Inferior vena cava|IVC]] by the tumor.<ref name="pmid30036602">{{cite journal |vauthors=De Campo JF |title=Ultrasound of Wilms' tumor |journal=Pediatr Radiol |volume=16 |issue=1 |pages=21–4 |date=1986 |pmid=3003660 |doi= |url=}}</ref>
|
*Findings on CT scan which can be suggestive of  wilms tumor include:<ref name="pmid4080660">{{cite journal |vauthors=Cahan LD |title=Failure of encephalo-duro-arterio-synangiosis procedure in moyamoya disease |journal=Pediatr Neurosci |volume=12 |issue=1 |pages=58–62 |date=1985 |pmid=4080660 |doi= |url=}}</ref>
**Heterogeneous soft-tissue density masses
**These masses have frequent areas of calcification (~10%) and fat-density regions
**Lymph node metastasis
*CT scan of the renal mass can further reveal:
**Invasion of surrounding organs
**Thrombus in or occlusion of the renal vein and/or the inferior vena cava
**Abdominal lymph nodes and contralateral involvement
|
*Wilms tumor has a triphasic appearance.
*It is comprised of 3 types of cells:
**[[Stromal]]
**[[Epithelium|Epithelial]]
**[[Blastema|Blastemal]]
*All the 3 types are not required for the diagnosis of Wilms tumor.
*Primitive tubules and [[Glomerulus|glomeruli]] are often seen comprised of [[Cancer|neoplastic]] cells.
*Beckwith and Palmer reported in NWTS the different histopathologic types of Wilms tumor to categorize them based on prognosis.<ref name="pmid1978">{{cite journal |vauthors=Jolly RD, Stellwagen E, Babul J, Vodkaĭlo LV, Titov VL, Moldomusaev DM, Maianskiĭ AN |title=Mannosidosis of Angus Cattle: a prototype control program for some genetic diseases |journal=Adv Vet Sci Comp Med |volume=19 |issue=23 |pages=1–21 |date=November 1975 |pmid=1978 |doi= |url=}}</ref>


{{CMG}}; {{AE}}
*Spindled cell [[stroma]] surrounding abortive tubules and [[Glomerulus|glomeruli]] is characteristic.
*The stroma may include:
**Striated [[muscle]] [[cartilage]]
**[[bone]]
**[[Adipose tissue|Fat tissue]]
**[[Fibrous connective tissue|Fibrous tissue.]]
|
|-
|2.
|[[Clear cell sarcoma of the kidney|Clear cell sarcoma]]
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|3.
|[[Renal cell carcinoma]]
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|Ultrasound (US) may be helpful when CT scan results are equivocal. It is noteworthy to mention that not all renal cell carcinomas are detectable on ultrasound.
|Both CT and MRI may be used to detect neoplastic masses that may define renal cell carcinoma or metastasis of the primary cancer. CT scan and use of intravenous (IV) contrast is generally used for work-up and follow-up of patients with renal cell carcinoma.
|The histological pattern of renal cell carcinoma depends whether it is papillary, chromophobe or collecting duct renal cell carcinoma.
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|-
|4.
|[[Malignant rhabdoid tumor|Rhabdoid kidney disease]]
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* CT scan may be diagnostic of malignant rhabdoid tumor. Findings on CT scan suggestive of malignant rhabdoid tumor include a large, heterogenous, centrally located mass, which is lobulated with individual lobules separated by intervening areas of decreased attenuation, relating to either previous [[hemorrhage]] or [[necrosis]]. Enhancement is similarly heterogeneous. [[Calcification]] is relatively common, observed in 20-50% of cases and is typically linear and tends to outline tumur lobules.
|Malignant rhabdoid tumor is characterized by the round blue tumor cells of high cellularity composed of atypical cells with eccentric nuclei, small nucleoli, and abundant amounts of eosinophilic cytoplasm with frequent mitotic figures.
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|-
|5.
|[[Polycystic kidney disease]]
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==Overview==
Ultrasound may be helpful in the diagnosis of polycystic kidney disease. Findings on an ultrasound diagnostic of polycystic kidney disease include:<ref name="pmid25786098">{{cite journal |vauthors=Chapman AB, Devuyst O, Eckardt KU, Gansevoort RT, Harris T, Horie S, Kasiske BL, Odland D, Pei Y, Perrone RD, Pirson Y, Schrier RW, Torra R, Torres VE, Watnick T, Wheeler DC |title=Autosomal-dominant polycystic kidney disease (ADPKD): executive summary from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference |journal=Kidney Int. |volume=88 |issue=1 |pages=17–27 |date=July 2015 |pmid=25786098 |pmc=4913350 |doi=10.1038/ki.2015.59 |url=}}</ref><ref name="pmid18945943">{{cite journal |vauthors=Pei Y, Obaji J, Dupuis A, Paterson AD, Magistroni R, Dicks E, Parfrey P, Cramer B, Coto E, Torra R, San Millan JL, Gibson R, Breuning M, Peters D, Ravine D |title=Unified criteria for ultrasonographic diagnosis of ADPKD |journal=J. Am. Soc. Nephrol. |volume=20 |issue=1 |pages=205–12 |date=January 2009 |pmid=18945943 |pmc=2615723 |doi=10.1681/ASN.2008050507 |url=}}</ref>
 
*At least three unilateral or bilateral [[cysts]] in patients 15 - 39 years old
== Overview ==
*Atleast two [[cysts]] in each [[kidney]] in patients 40 - 59 years old
The clinical presentations of hypersensitivity pneumonitis depend on the frequency, length, exposure, and duration of illness. Due to a lot of variation in the the presentation hypersensitivity pneumonitis has been classified according to various schemes. Hypersensitivity pneumonitis may be classified into several subtypes based on various classifications methods such as classical classification, boyd classification, cormier classification, and selman classification.
*Atleast four [[cysts]] in each [[kidney]] in patients 60 years of age or older
|


== Classification ==
[[Renal]] CT scan may be helpful in the diagnosis of polycystic kidney disease. Findings on CT scan diagnostic of ADPKD include:
* The clinical presentations of hypersensitivity pneumonitis depend on:
* Numerous [[renal]] [[cysts]] of varying size and shape with little intervening [[parenchyma]] with water [[attenuation]] and very thin wall.
** Frequency
* Reduction in [[sinus]] [[fat]] due to expansion of the [[cortex]]
** Length
* Occasional complex [[cysts]] with hyperdense appearance, with possible septations or calcifications
** Exposure
* Multiple [[homogeneous]] and hypoattenuating [[cystic]] lesions in the [[liver]] in patients with [[liver]] involvement
** Duration of illness
|
* Due to a lot of variation in the the presentation hypersensitivity pneumonitis has been classified according to various schemes.
*On microscopic histopathological analysis, interstitial fibrosis, tubular atrophy, thickening and lamellation of tubular basement membranes, microcysts and negative immunofluorescence for complement and immunoglobulin are characteristic findings of ADPKD.<ref name="pmid12234310">{{cite journal |vauthors=Stavrou C, Koptides M, Tombazos C, Psara E, Patsias C, Zouvani I, Kyriacou K, Hildebrandt F, Christofides T, Pierides A, Deltas CC |title=Autosomal-dominant medullary cystic kidney disease type 1: clinical and molecular findings in six large Cypriot families |journal=Kidney Int. |volume=62 |issue=4 |pages=1385–94 |date=October 2002 |pmid=12234310 |doi=10.1111/j.1523-1755.2002.kid581.x |url=}}</ref><ref name="pmid24509297">{{cite journal |vauthors=Bleyer AJ, Kmoch S, Antignac C, Robins V, Kidd K, Kelsoe JR, Hladik G, Klemmer P, Knohl SJ, Scheinman SJ, Vo N, Santi A, Harris A, Canaday O, Weller N, Hulick PJ, Vogel K, Rahbari-Oskoui FF, Tuazon J, Deltas C, Somers D, Megarbane A, Kimmel PL, Sperati CJ, Orr-Urtreger A, Ben-Shachar S, Waugh DA, McGinn S, Bleyer AJ, Hodanová K, Vylet'al P, Živná M, Hart TC, Hart PS |title=Variable clinical presentation of an MUC1 mutation causing medullary cystic kidney disease type 1 |journal=Clin J Am Soc Nephrol |volume=9 |issue=3 |pages=527–35 |date=March 2014 |pmid=24509297 |pmc=3944763 |doi=10.2215/CJN.06380613 |url=}}</ref><ref name="pmid21775974">{{cite journal |vauthors=Faguer S, Decramer S, Chassaing N, Bellanné-Chantelot C, Calvas P, Beaufils S, Bessenay L, Lengelé JP, Dahan K, Ronco P, Devuyst O, Chauveau D |title=Diagnosis, management, and prognosis of HNF1B nephropathy in adulthood |journal=Kidney Int. |volume=80 |issue=7 |pages=768–76 |date=October 2011 |pmid=21775974 |doi=10.1038/ki.2011.225 |url=}}</ref><ref name="pmid20378641">{{cite journal |vauthors=Heidet L, Decramer S, Pawtowski A, Morinière V, Bandin F, Knebelmann B, Lebre AS, Faguer S, Guigonis V, Antignac C, Salomon R |title=Spectrum of HNF1B mutations in a large cohort of patients who harbor renal diseases |journal=Clin J Am Soc Nephrol |volume=5 |issue=6 |pages=1079–90 |date=June 2010 |pmid=20378641 |pmc=2879303 |doi=10.2215/CJN.06810909 |url=}}</ref>
* Hypersensitivity pneumonitis may be classified into several subtypes based on:
** '''Classical classification''':
*** Acute
**** Abrupt in onset.
**** Occurs after heavy exposure to antigen.
**** Symptoms can be confused with bacterial or viral infection.
**** On auscultation diffuse crackles and tachypnea are notable.
**** Histopathology reveals non-caseating interstitial granulomas with giant cells. 
*** Subacute
**** Gradual in onset.
**** Symptom like cough, fatigue, weightloss, and dyspnea may be seen.
**** Removal of exposure leads to complete resolution.
**** On auscultation diffuse crackles and tachypnea may be seen.
**** Histopathology reveals more well formed non-caseating interstitial granulomas and interstitial fibrosis.
*** Chronic
**** Insidious in onset with history of acute episodes.
**** Digital clubbing may be seen. 
**** Pulmonary fibrosis leads to disabling and irreversible respiratory symptoms.
** '''Boyd classification''':
*** Acute progressive
**** Severe symptoms occur after exposure to antigen.
**** Recurrent exposure leads to symptom progression.
**** Clinically patients are pyrexial with bilateral crackles on chest auscultation.
**** Patients may require hospitalization due to respiratory compromise.
*** Acute intermittent nonprogressive
**** Similar to acute progressive disease but less intense.
**** Patients feel well in between episodes.
**** Subsequent exposure leads to less severe symptoms.
**** Patients are clinically stable in the long run.
**** Pulmonary inflammatory response deteriorates with recurrent exposure to the antigen.
*** Chronic progressive disease
**** Occurs after recurrent acute episodes or insidiously.
**** Patients are diagnosed in the late stages.
**** Only clue for diagnosis is antigen exposure.
**** Patients often present with permanent disability in the form of pulmonary fibrosis or respiratory failure.
**** Disease is not reversed even after antigen exposure is avoided. 
*** Subclinical disease
**** Patients are immunological sensitized but are asymptomatic.
**** Patients with recurrent exposure to antigens may convert to chronic form.
** '''Cormier classification''':
*** Active
*** Residual
** '''Selman classification''':
*** Active non-progressive and intermittent
*** Acute progressive and intermittent
*** Chronic
**** Nonprogressive
**** Progressive


=== Prevalence ===
* sThe prevalence of hypersensitivity pneumonitis varies based on exposure/occupation.
* These are as following:
**Farmers:
*** US: 8-540 cases per 100,000 persons per year among those at risk.<ref name="pmid7027852">{{cite journal |vauthors=Gruchow HW, Hoffmann RG, Marx JJ, Emanuel DA, Rimm AA |title=Precipitating antibodies to farmer's lung antigens in a Wisconsin farming population |journal=Am. Rev. Respir. Dis. |volume=124 |issue=4 |pages=411–5 |year=1981 |pmid=7027852 |doi=10.1164/arrd.1981.124.4.411 |url=}}</ref>
*** UK: 420-3000 cases per 100,000 persons per year among those at risk.<ref name="pmid8217855">{{cite journal |vauthors=Dalphin JC, Debieuvre D, Pernet D, Maheu MF, Polio JC, Toson B, Dubiez A, Monnet E, Laplante JJ, Depierre A |title=Prevalence and risk factors for chronic bronchitis and farmer's lung in French dairy farmers |journal=Br J Ind Med |volume=50 |issue=10 |pages=941–4 |year=1993 |pmid=8217855 |pmc=1035525 |doi= |url=}}</ref>
*** France: 4370 cases per 100,000 persons per year among those at risk.<ref name="pmid3420554">{{cite journal |vauthors=Depierre A, Dalphin JC, Pernet D, Dubiez A, Faucompré C, Breton JL |title=Epidemiological study of farmer's lung in five districts of the French Doubs province |journal=Thorax |volume=43 |issue=6 |pages=429–35 |year=1988 |pmid=3420554 |pmc=461305 |doi= |url=}}</ref>
*** Finland: 1400-1700 cases per 100,000 persons per year among those at risk.<ref name="pmid2220830">{{cite journal |vauthors=Terho EO |title=Work-related respiratory disorders among Finnish farmers |journal=Am. J. Ind. Med. |volume=18 |issue=3 |pages=269–72 |year=1990 |pmid=2220830 |doi= |url=}}</ref>
** Pigeon Breeders: 6000-21,000 cases per 100,000 persons per year
** Bird Fanciers: 20-20,000 cases per 100,000 persons per year


===Age===
|
* Hypersensitivity pneumonitis usually affects patients in fourth to sixth decade of life.
|-
* The mean age at diagnosis is 53 +/- 14 years.<ref name="pmid176059602">{{cite journal |vauthors=Hanak V, Golbin JM, Ryu JH |title=Causes and presenting features in 85 consecutive patients with hypersensitivity pneumonitis |journal=Mayo Clin. Proc. |volume=82 |issue=7 |pages=812–6 |year=2007 |pmid=17605960 |doi=10.4065/82.7.812 |url=}}</ref>
|6.
|[[Pheochromocytoma]]
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|The following findings may be observed on [[CT scan]]:<ref name="pmid1787652">{{cite journal| author=Bravo EL| title=Pheochromocytoma: new concepts and future trends. | journal=Kidney Int | year= 1991 | volume= 40 | issue= 3 | pages= 544-56 | pmid=1787652 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1787652 }}</ref>
*Most common extra-[[Adrenal gland|adrenal]] locations are superior and inferior [[abdominal]] [[Paraaortic lymph node|paraaortic]] areas, the [[urinary bladder]], [[thorax]], [[head]], [[neck]] and [[pelvis]].<ref name="pmid1729490">{{cite journal| author=Whalen RK, Althausen AF, Daniels GH| title=Extra-adrenal pheochromocytoma. | journal=J Urol | year= 1992 | volume= 147 | issue= 1 | pages= 1-10 | pmid=1729490 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1729490  }}</ref>


=== Race ===
*In sporadic pheochromocytoma, [[CT]] and [[MRI]] are good choices. The choice depends on availability and cost.<ref name="pmid191248172">{{cite journal| author=Baid SK, Lai EW, Wesley RA, Ling A, Timmers HJ, Adams KT et al.| title=Brief communication: radiographic contrast infusion and catecholamine release in patients with pheochromocytoma. | journal=Ann Intern Med | year= 2009 | volume= 150 | issue= 1 | pages= 27-32 | pmid=19124817 | doi= | pmc=3490128 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19124817  }}</ref>
* There is no racial predilection to hypersensitivity pneumonitis.
*In patients with the [[multiple endocrine neoplasia]] type 2 ([[Multiple endocrine neoplasia type 2|MEN2]]) syndrome, [[CT]] may miss the [[tumors]].<ref name="pmid17876522">{{cite journal| author=Bravo EL| title=Pheochromocytoma: new concepts and future trends. | journal=Kidney Int | year= 1991 | volume= 40 | issue= 3 | pages= 544-56 | pmid=1787652 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1787652  }}</ref>
|On microscopic pathology, Pheochromocytoma typically demonstrates a nesting (Zellballen) pattern on microscopy. This pattern is composed of well-defined clusters of tumor cells containing eosinophilic cytoplasm separated by fibrovascular stroma.
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|7.
|[[Burkitt's lymphoma|Burkitt lymphoma]]
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|Abdominal US may show splenomegaly and ascites.
|Chest, abdomen, and pelvis [[CT]] scan may be helpful in the diagnosis of Burkitt's lymphoma but it is not done routinely.<ref name="medlineplus">Burkitt lymphoma. MedlinePlus. https://www.nlm.nih.gov/medlineplus/ency/article/001308.htm Accessed on September 30, 2015</ref>
|
*On microscopic histopathological analysis, characteristic findings of Burkitt's lymphoma include:<ref name="pmid12610094">{{cite journal |author=Bellan C, Lazzi S, De Falco G, Nyongo A, Giordano A, Leoncini L |title=Burkitt's lymphoma: new insights into molecular pathogenesis |journal=J. Clin. Pathol. |volume=56 |issue=3 |pages=188–92 |year=2003 |month=March |pmid=12610094 |pmc=1769902 |doi= |url=http://jcp.bmj.com/cgi/pmidlookup?view=long&pmid=12610094}}</ref>
:*Medium-sized (~1.5-2x the size of a RBC) with uniform size ("monotonous") -- '''key feature''' (i.e. tumor nuclei size similar to that of [[histiocytes]] or [[endothelial cells]])
:*Round nucleus
:*Small nucleoli
:*Relatively abundant cytoplasm ([[basophilic]])
:*Brisk mitotic rate and [[apoptotic]] activity
:*Cellular outline usually appears squared off
:*"Starry-sky pattern":
::*The ''stars'' in the pattern are tingible-body macrophages (macrophages containing [[apoptotic]] tumor cells)


=== Gender===
::*The tumour cells are the ''sky''
* Hypersensitivity pneumonitis affects men and women equally.
|
* Death due to Hypersensitivity pneumonitis is reported more in men.<ref>Adkinson NF. Hypersensitivity Pneumonitis. ''Middleton's Allergy: Principles and Practice''. 8th Ed. Saunders; 2013.</ref>
|-
 
|8.
== Pathophysiology of Oral Cancer ==
|[[Intussusception]]
 
|
=== Tumor suppressor genes (TSGs) ===
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* It is understood that oral cavity cancer is the result of allelic imbalance which is caused by chromosomal changes particularly in chromosome 3,9,11 and 17.
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* These changes lead to mutation in tumor suppressor genes (TSGs).  
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* Normally TSGs modulate normal growth.
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* Mutation of these TSGs leads to dysfunctional growth control.
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* Mutation most commonly occurs in either of the following:
* [[Ultrasound]] is the [[Gold standard (test)|gold standard]] imaging modality used to diagnose intussusception<ref name="pmid17308922">{{cite journal |vauthors=Ko HS, Schenk JP, Tröger J, Rohrschneider WK |title=Current radiological management of intussusception in children |journal=Eur Radiol |volume=17 |issue=9 |pages=2411–21 |year=2007 |pmid=17308922 |doi=10.1007/s00330-007-0589-y |url=}}</ref>
** Short arm of chromosome 3
**Target or doughnut sign<ref name="pmid8470658">{{cite journal |vauthors=Boyle MJ, Arkell LJ, Williams JT |title=Ultrasonic diagnosis of adult intussusception |journal=Am. J. Gastroenterol. |volume=88 |issue=4 |pages=617–8 |year=1993 |pmid=8470658 |doi= |url=}}</ref>
** TSG termed ''P16'' on chromosome 9
***Edematous intussuscipien forms an external ring around the centrally located intussusceptum
** TSG termed ''TP53'' on chromosome 17
***Target sign is usually seen in right lower quadrant
* Cytochrome P450 genotypes is related to mutations in some TSGs  and lead to oral squamous cell carcinoma.
**Layers of intussusception forms pseudo-kidney appearance on the transverse view
* In western countries (eg, United Kingdom, United States, Australia) ''TP53'' [[Mutation|mutations]] are the most common molecular change that leads to oral [[squamous cell carcinoma]].
|
 
* [[Computed tomography|CT scan]] may be helpful in the [[diagnosis]] of intussusception. [[Computed tomography|CT scan]] maybe used when other image modalities like [[x-ray]] and [[ultrasound]] have not given positive results but suspicion of intussusception is high.
=== Oncogenes ===
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* Cancer may also occur if there is mutation to other genes that control cell growth, mainly oncogenes.
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* Oncogenes most commonly involved are:
|-
** Chromosome 11 (''PRAD1)''
|9.
** Chromosome 17 (Harvey ras [H-''ras''])
|[[Hydronephrosis]]
* In eastern countries (eg, India, Southeast Asia), ''ras'' [[oncogenes]] is a more common cause of oral squamous cell carcinoma.  
|
 
|
=== Carcinogen-metabolizing enzymes ===
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* Carcinogen-metabolizing enzymes are known to cause cancer in some patients.
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* Cytotoxic enzymes such as alcohol dehydrogenase result in the production of:
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** Free radicles
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** DNA hydroxylated bases
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* These cytotoxic enzymes especially predispose oral squamous cell carcinoma.
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=== Alcohol ===
|-
* Alcohol dehydrogenase oxidizes ethanol to acetaldehyde which is cytotoxic in nature.
|10.
* cytochrome P450 IIEI (CYP2E1) also metabolizes ethanol to acetaldehyde.
|[[Renal cyst]]
* Alcohol dehydrogenase type 3 genotype predisposes to oral squamous cell carcinoma.
|
* Carcinogenic potential increases when combined with tobacco use.
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=== Tobacco ===
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* Cigarette smoke has various carcinogens which can lead to oral cancers.
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* Low reactive free radicals in cigarette smoke interact with redox-active metals in saliva.  
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* This makes saliva to loose its antioxidant potential and become a potent pro-oxidant milieu.<ref name="pmid17344667">{{cite journal |vauthors=Nagler R, Dayan D |title=The dual role of saliva in oral carcinogenesis |journal=Oncology |volume=71 |issue=1-2 |pages=10–7 |year=2006 |pmid=17344667 |doi=10.1159/000100445 |url=}}</ref>
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==Gross Pathological Findings==
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|-
Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. [http://www.peir.net © PEIR, University of Alabama at Birmingham, Department of Pathology]
|11.
 
|Renal thrombosis
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==References==
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{{reflist|2}}
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|12.
{{Metabolic pathology}}
|[[Dysplasia|Dysplastic kidney]]
 
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[[Category:Hepatology]]
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|13.
|[[Hemorrhage|Renal hemorrhage]]
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|14.
|[[Neuroblastoma|Pediatric Neuroblastoma]]
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|15.
|[[Rhabdomyosarcoma|Pediatric Rhabdomyosarcoma]]
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|16.
|[[Mesoblastic nephroma]]
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|Most common renal tumor that occurs in 1st month of life
|}

Latest revision as of 20:31, 21 June 2018


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2]

Differential Diagnosis

S.No. Disease Symptoms Signs Diagnosis Comments
Abdominal Pain Hematuria Headache Abdominal mass Abdominal tenderness Ultrasonography CT scan Histology
1. Wilms tumor + + - + +
  • It is the best initial diagnostic study used in cases suspected with wilms tumor.
  • Ultrasonography can help identify the mass as a kidney mass.
  • It can distinguish tumor mass from other causes of renal swelling like hydronephrosis.[1]
  • Doppler ultrasonography can help to detect invasion of renal vein and IVC by the tumor.[2]
  • Findings on CT scan which can be suggestive of wilms tumor include:[3]
    • Heterogeneous soft-tissue density masses
    • These masses have frequent areas of calcification (~10%) and fat-density regions
    • Lymph node metastasis
  • CT scan of the renal mass can further reveal:
    • Invasion of surrounding organs
    • Thrombus in or occlusion of the renal vein and/or the inferior vena cava
    • Abdominal lymph nodes and contralateral involvement
  • Wilms tumor has a triphasic appearance.
  • It is comprised of 3 types of cells:
  • All the 3 types are not required for the diagnosis of Wilms tumor.
  • Primitive tubules and glomeruli are often seen comprised of neoplastic cells.
  • Beckwith and Palmer reported in NWTS the different histopathologic types of Wilms tumor to categorize them based on prognosis.[4]
2. Clear cell sarcoma
3. Renal cell carcinoma Ultrasound (US) may be helpful when CT scan results are equivocal. It is noteworthy to mention that not all renal cell carcinomas are detectable on ultrasound. Both CT and MRI may be used to detect neoplastic masses that may define renal cell carcinoma or metastasis of the primary cancer. CT scan and use of intravenous (IV) contrast is generally used for work-up and follow-up of patients with renal cell carcinoma. The histological pattern of renal cell carcinoma depends whether it is papillary, chromophobe or collecting duct renal cell carcinoma.
4. Rhabdoid kidney disease
  • CT scan may be diagnostic of malignant rhabdoid tumor. Findings on CT scan suggestive of malignant rhabdoid tumor include a large, heterogenous, centrally located mass, which is lobulated with individual lobules separated by intervening areas of decreased attenuation, relating to either previous hemorrhage or necrosis. Enhancement is similarly heterogeneous. Calcification is relatively common, observed in 20-50% of cases and is typically linear and tends to outline tumur lobules.
 Malignant rhabdoid tumor is characterized by the round blue tumor cells of high cellularity composed of atypical cells with eccentric nuclei, small nucleoli, and abundant amounts of eosinophilic cytoplasm with frequent mitotic figures.
5. Polycystic kidney disease

Ultrasound may be helpful in the diagnosis of polycystic kidney disease. Findings on an ultrasound diagnostic of polycystic kidney disease include:[5][6]

  • At least three unilateral or bilateral cysts in patients 15 - 39 years old
  • Atleast two cysts in each kidney in patients 40 - 59 years old
  • Atleast four cysts in each kidney in patients 60 years of age or older

Renal CT scan may be helpful in the diagnosis of polycystic kidney disease. Findings on CT scan diagnostic of ADPKD include:

  • Numerous renal cysts of varying size and shape with little intervening parenchyma with water attenuation and very thin wall.
  • Reduction in sinus fat due to expansion of the cortex
  • Occasional complex cysts with hyperdense appearance, with possible septations or calcifications
  • Multiple homogeneous and hypoattenuating cystic lesions in the liver in patients with liver involvement
  • On microscopic histopathological analysis, interstitial fibrosis, tubular atrophy, thickening and lamellation of tubular basement membranes, microcysts and negative immunofluorescence for complement and immunoglobulin are characteristic findings of ADPKD.[7][8][9][10]
6. Pheochromocytoma The following findings may be observed on CT scan:[11] On microscopic pathology, Pheochromocytoma typically demonstrates a nesting (Zellballen) pattern on microscopy. This pattern is composed of well-defined clusters of tumor cells containing eosinophilic cytoplasm separated by fibrovascular stroma.
7. Burkitt lymphoma Abdominal US may show splenomegaly and ascites. Chest, abdomen, and pelvis CT scan may be helpful in the diagnosis of Burkitt's lymphoma but it is not done routinely.[15]
  • On microscopic histopathological analysis, characteristic findings of Burkitt's lymphoma include:[16]
  • Medium-sized (~1.5-2x the size of a RBC) with uniform size ("monotonous") -- key feature (i.e. tumor nuclei size similar to that of histiocytes or endothelial cells)
  • Round nucleus
  • Small nucleoli
  • Relatively abundant cytoplasm (basophilic)
  • Brisk mitotic rate and apoptotic activity
  • Cellular outline usually appears squared off
  • "Starry-sky pattern":
  • The stars in the pattern are tingible-body macrophages (macrophages containing apoptotic tumor cells)
  • The tumour cells are the sky
8. Intussusception
  • Ultrasound is the gold standard imaging modality used to diagnose intussusception[17]
    • Target or doughnut sign[18]
      • Edematous intussuscipien forms an external ring around the centrally located intussusceptum
      • Target sign is usually seen in right lower quadrant
    • Layers of intussusception forms pseudo-kidney appearance on the transverse view
  • CT scan may be helpful in the diagnosis of intussusception. CT scan maybe used when other image modalities like x-ray and ultrasound have not given positive results but suspicion of intussusception is high.
9. Hydronephrosis
10. Renal cyst
11. Renal thrombosis
12. Dysplastic kidney
13. Renal hemorrhage
14. Pediatric Neuroblastoma
15. Pediatric Rhabdomyosarcoma
16. Mesoblastic nephroma Most common renal tumor that occurs in 1st month of life
  1. ↑ Hartman DS, Sanders RC (April 1982). "Wilms' tumor versus neuroblastoma: usefulness of ultrasound in differentiation". J Ultrasound Med. 1 (3): 117–22. PMID 6152936.
  2. ↑ De Campo JF (1986). "Ultrasound of Wilms' tumor". Pediatr Radiol. 16 (1): 21–4. PMID 3003660.
  3. ↑ Cahan LD (1985). "Failure of encephalo-duro-arterio-synangiosis procedure in moyamoya disease". Pediatr Neurosci. 12 (1): 58–62. PMID 4080660.
  4. ↑ Jolly RD, Stellwagen E, Babul J, Vodkaĭlo LV, Titov VL, Moldomusaev DM, Maianskiĭ AN (November 1975). "Mannosidosis of Angus Cattle: a prototype control program for some genetic diseases". Adv Vet Sci Comp Med. 19 (23): 1–21. PMID 1978.
  5. ↑ Chapman AB, Devuyst O, Eckardt KU, Gansevoort RT, Harris T, Horie S, Kasiske BL, Odland D, Pei Y, Perrone RD, Pirson Y, Schrier RW, Torra R, Torres VE, Watnick T, Wheeler DC (July 2015). "Autosomal-dominant polycystic kidney disease (ADPKD): executive summary from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference". Kidney Int. 88 (1): 17–27. doi:10.1038/ki.2015.59. PMC 4913350. PMID 25786098.
  6. ↑ Pei Y, Obaji J, Dupuis A, Paterson AD, Magistroni R, Dicks E, Parfrey P, Cramer B, Coto E, Torra R, San Millan JL, Gibson R, Breuning M, Peters D, Ravine D (January 2009). "Unified criteria for ultrasonographic diagnosis of ADPKD". J. Am. Soc. Nephrol. 20 (1): 205–12. doi:10.1681/ASN.2008050507. PMC 2615723. PMID 18945943.
  7. ↑ Stavrou C, Koptides M, Tombazos C, Psara E, Patsias C, Zouvani I, Kyriacou K, Hildebrandt F, Christofides T, Pierides A, Deltas CC (October 2002). "Autosomal-dominant medullary cystic kidney disease type 1: clinical and molecular findings in six large Cypriot families". Kidney Int. 62 (4): 1385–94. doi:10.1111/j.1523-1755.2002.kid581.x. PMID 12234310.
  8. ↑ Bleyer AJ, Kmoch S, Antignac C, Robins V, Kidd K, Kelsoe JR, Hladik G, Klemmer P, Knohl SJ, Scheinman SJ, Vo N, Santi A, Harris A, Canaday O, Weller N, Hulick PJ, Vogel K, Rahbari-Oskoui FF, Tuazon J, Deltas C, Somers D, Megarbane A, Kimmel PL, Sperati CJ, Orr-Urtreger A, Ben-Shachar S, Waugh DA, McGinn S, Bleyer AJ, Hodanová K, Vylet'al P, Živná M, Hart TC, Hart PS (March 2014). "Variable clinical presentation of an MUC1 mutation causing medullary cystic kidney disease type 1". Clin J Am Soc Nephrol. 9 (3): 527–35. doi:10.2215/CJN.06380613. PMC 3944763. PMID 24509297.
  9. ↑ Faguer S, Decramer S, Chassaing N, Bellanné-Chantelot C, Calvas P, Beaufils S, Bessenay L, Lengelé JP, Dahan K, Ronco P, Devuyst O, Chauveau D (October 2011). "Diagnosis, management, and prognosis of HNF1B nephropathy in adulthood". Kidney Int. 80 (7): 768–76. doi:10.1038/ki.2011.225. PMID 21775974.
  10. ↑ Heidet L, Decramer S, Pawtowski A, Morinière V, Bandin F, Knebelmann B, Lebre AS, Faguer S, Guigonis V, Antignac C, Salomon R (June 2010). "Spectrum of HNF1B mutations in a large cohort of patients who harbor renal diseases". Clin J Am Soc Nephrol. 5 (6): 1079–90. doi:10.2215/CJN.06810909. PMC 2879303. PMID 20378641.
  11. ↑ Bravo EL (1991). "Pheochromocytoma: new concepts and future trends". Kidney Int. 40 (3): 544–56. PMID 1787652.
  12. ↑ Whalen RK, Althausen AF, Daniels GH (1992). "Extra-adrenal pheochromocytoma". J Urol. 147 (1): 1–10. PMID 1729490.
  13. ↑ Baid SK, Lai EW, Wesley RA, Ling A, Timmers HJ, Adams KT; et al. (2009). "Brief communication: radiographic contrast infusion and catecholamine release in patients with pheochromocytoma". Ann Intern Med. 150 (1): 27–32. PMC 3490128. PMID 19124817.
  14. ↑ Bravo EL (1991). "Pheochromocytoma: new concepts and future trends". Kidney Int. 40 (3): 544–56. PMID 1787652.
  15. ↑ Burkitt lymphoma. MedlinePlus. https://www.nlm.nih.gov/medlineplus/ency/article/001308.htm Accessed on September 30, 2015
  16. ↑ Bellan C, Lazzi S, De Falco G, Nyongo A, Giordano A, Leoncini L (2003). "Burkitt's lymphoma: new insights into molecular pathogenesis". J. Clin. Pathol. 56 (3): 188–92. PMC 1769902. PMID 12610094. Unknown parameter |month= ignored (help)
  17. ↑ Ko HS, Schenk JP, Tröger J, Rohrschneider WK (2007). "Current radiological management of intussusception in children". Eur Radiol. 17 (9): 2411–21. doi:10.1007/s00330-007-0589-y. PMID 17308922.
  18. ↑ Boyle MJ, Arkell LJ, Williams JT (1993). "Ultrasonic diagnosis of adult intussusception". Am. J. Gastroenterol. 88 (4): 617–8. PMID 8470658.
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